Pathways linking activity, adiposity, and inflammation to bone mineral density in women and men from NHANES 2007 to 2010.

OBJECTIVES: Age, sedentary activity, central adiposity, and inflammation have all been independently associated with bone mineral density (BMD). We assessed how the effects of sedentary activity and central adiposity on BMD of the lumbar spine and femoral neck change across early to late adulthood and whether these relationships are mediated by inflammation. METHODS: We analyzed data from 7135 women and men 20 years of age and older from NHANES 2007 to 2010. Anthropometrics, sedentary activity (min/day), serum CRP (mg/dl), and BMD (gm/cm2 measured by DXA scans) at the femoral neck and lumbar spine. Data were compared by age and sex groups and through causal mediation analysis. RESULTS: The effect of waist circumference on BMD was significantly mediated by serum CRP at both skeletal sites in men and at the femoral neck in women. Sedentary activity did not have a direct relationship to BMD but was mediated by waist circumference in men. Least square means differed significantly by sex and age groups with a general age-related decline in BMD at both skeletal sites. CONCLUSIONS: We found that central adiposity, independent of overall body size and composition as measured through BMI, has an inverse relationship with BMD that is mediated by serum CRP. In addition, the negative impact of increased sedentism acted through changes in central adiposity (waist circumference) but only in men. Although low bone density and osteoporosis are often considered degenerative diseases that primarily impact postmenopausal women, our findings show that sedentary activity and central adiposity impact bone density beginning in early adulthood in both women and men.

Biocultural pathways linking periodontal disease expression to food insecurity, immune dysregulation, and nutrition.

OBJECTIVES: In this article, we test theoretical pathways leading to and resulting from periodontal disease to better understand how periodontal disease, which is measurable in both past and present populations, integrates biocultural context and affects whole-body physiology. METHODS: We use data from the National Health and Nutrition Examination Survey (NHANES) 2003-2004 and logistic and linear regressions to test pathways linking psychosocial stress to periodontal disease, and periodontal disease to serum vitamin C levels. We then use causal mediation analysis to test the role of mediating variables in these pathways (n = 1853 individuals). RESULTS: Food insecurity was positively associated with periodontal disease and negatively associated with serum counts of C-reactive protein (CRP) and neutrophils. Neither CRP nor neutrophils significantly mediated the relationship between food insecurity and periodontal disease. Periodontal disease was negatively associated with serum vitamin C levels and positively associated with neutrophil counts. Neutrophils may mediate the relationship between periodontal disease and vitamin C. CONCLUSIONS: We identify two main findings: (a) periodontal disease contributes to and may result from immune dysregulation, particularly of neutrophils, and (b) an immune response to chronic infection such as periodontal disease is metabolically expensive for the body to maintain and likely depletes serum micronutrient levels. Both micronutrient status and serum neutrophil counts affect multiple skeletal and physiological phenotypes and thus position periodontal disease in whole-body context.